Luo Jiajia, Chen Luyun, Fenner Dee E, Ashton-Miller James A, DeLancey John O L
Pelvic Floor Research Group, University of Michigan, Ann Arbor, MI, USA; Biomechanics Research Laboratory, Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI, USA.
Pelvic Floor Research Group, University of Michigan, Ann Arbor, MI, USA; Biomechanics Research Laboratory, Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI, USA.
J Biomech. 2015 Jun 25;48(9):1580-6. doi: 10.1016/j.jbiomech.2015.02.041. Epub 2015 Feb 26.
We developed a subject-specific 3-D finite element model to understand the mechanics underlying formation of female pelvic organ prolapse, specifically a rectocele and its interaction with a cystocele. The model was created from MRI 3-D geometry of a healthy 45 year-old multiparous woman. It included anterior and posterior vaginal walls, levator ani muscle, cardinal and uterosacral ligaments, anterior and posterior arcus tendineus fascia pelvis, arcus tendineus levator ani, perineal body, perineal membrane and anal sphincter. Material properties were mostly from the literature. Tissue impairment was modeled as decreased tissue stiffness based on previous clinical studies. Model equations were solved using Abaqus v 6.11. The sensitivity of anterior and posterior vaginal wall geometry was calculated for different combinations tissue impairments under increasing intraabdominal pressure. Prolapse size was reported as pelvic organ prolapse quantification system (POP-Q) point at point Bp for rectocele and point Ba for cystocele. Results show that a rectocele resulted from impairments of the levator ani and posterior compartment support. For 20% levator and 85% posterior support impairments, simulated rectocele size (at POP-Q point: Bp) increased 0.29 mm/cm H2O without apical impairment and 0.36 mm/cm H2O with 60% apical impairment, as intraabdominal pressures increased from 0 to 150 cm H2O. Apical support impairment could result in the development of either a cystocele or rectocele. Simulated repair of posterior compartment support decreased rectocele but increased a preexisting cystocele. We conclude that development of rectocele and cystocele depend on the presence of anterior, posterior, levator and/or or apical support impairments, as well as the interaction of the prolapse with the opposing compartment.
我们开发了一个针对个体的三维有限元模型,以了解女性盆腔器官脱垂,特别是直肠膨出的形成机制及其与膀胱膨出的相互作用。该模型基于一名45岁经产妇的健康MRI三维几何结构创建。它包括阴道前壁和后壁、肛提肌、主韧带和子宫骶韧带、盆筋膜弓状线前后部、肛提肌腱弓、会阴体、会阴膜和肛门括约肌。材料属性大多来自文献。根据先前的临床研究,将组织损伤模拟为组织刚度降低。使用Abaqus v 6.11求解模型方程。在腹内压升高的情况下,计算了不同组织损伤组合下阴道前壁和后壁几何形状的敏感性。脱垂大小以盆腔器官脱垂量化系统(POP-Q)在直肠膨出的Bp点和膀胱膨出的Ba点进行报告。结果表明,直肠膨出是由肛提肌和后盆腔支持结构损伤引起的。当腹内压从0增加到150 cm H2O时,对于20%的肛提肌损伤和85%的后盆腔支持结构损伤,在无顶端损伤时,模拟的直肠膨出大小(在POP-Q点:Bp)增加0.29 mm/cm H2O,在有60%顶端损伤时增加0.36 mm/cm H2O。顶端支持结构损伤可能导致膀胱膨出或直肠膨出的发生。模拟修复后盆腔支持结构可减少直肠膨出,但会增加已有的膀胱膨出。我们得出结论,直肠膨出和膀胱膨出的发生取决于前、后、肛提肌和/或顶端支持结构损伤的存在,以及脱垂与相对盆腔的相互作用。